ReviewHeliyon2023
IL-1β-mediated inflammatory responses in intervertebral disc degeneration: Mechanisms, signaling pathways, and therapeutic potential.
Review in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Glucagon-like peptide-1: a critical link between gut microbiota dysbiosis and degenerative musculoskeletal diseases.Gut microbes · 2026Review
- Current research on the role of HIF in intervertebral disc degeneration.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Review
- Epithelial-dermal inflammasome crosstalk in cutaneous squamous cell carcinoma.Molecular biology of the cell · 2026Article
- HACE1 alleviates intervertebral disc degeneration by inhibiting ferroptosis in nucleus pulposus cells.Scientific reports · 2026Article
- Article
- Association Between the Expression of T Helper Type 17 Cell-Related Cytokines and Valve Damage in Rheumatic Heart Disease.Molecular biotechnology · 2025Article
- Modulating NLRP3 Inflammasomes in Idiopathic Pulmonary Fibrosis: A Comprehensive Review on Flavonoid-Based Interventions.Cell biochemistry and biophysics · 2025Review
- Potential diagnostic and therapeutic gene in chronic low back pain through pyroptosis modulation: A silico study based on the dataset analysis.Scientific reports · 2025Article
- Mechanisms and Therapeutic Strategies of Macrophage Polarization in Intervertebral Disc Degeneration.JOR spine · 2025Review
- Role of macrophage in intervertebral disc degeneration.Bone research · 2025Review
- The Role of Microvascular Variations in the Process of Intervertebral Disk Degeneration and Its Regulatory Mechanisms: A Literature Review.Orthopaedic surgery · 2024Review
- Discogenic Low Back Pain: Anatomic and Pathophysiologic Characterization, Clinical Evaluation, Biomarkers, AI, and Treatment Options.Journal of clinical medicine · 2024Review
- Custom-Made Ce-Mn Bimetallic Nanozyme for the Treatment of Intervertebral Disc Degeneration by Inhibiting Oxidative Stress and Modulating Macrophage M1/M2 Polarization.Biomaterials research · 2024Article
- Causal relationship of interferon-γ and interleukin-18 upstream of intervertebral disc degeneration pathogenesis: a two-sample Mendelian randomization study.Frontiers in neurology · 2024Article
- Efficacy of Medical Ozone as an Adjuvant Treatment in Dogs with Intervertebral Disc Protusions-A Retrospective Study.Animals : an open access journal from MDPI · 2023Article
Corrections and comments
- Retraction · 2025-08-07Concerns/Issues about Authorship/Affiliation · Duplication of/in Article · Euphemisms for Duplication · Investigation by Journal/Publisher ·
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD) has been widely recognized as the primary cause of low back pain and is one of the major chronic diseases imposing a severe socioeconomic burden worldwide. IDD is a degenerative process characterized by inflammatory responses, and its underlying pathological mechanisms remain complex. Genetic, developmental, biochemical, and biomechanical factors contribute to the development of IDD. There is a pressing need for an effective non-surgical treatment, mainly due to the lack of comprehensive understanding of the specific mechanisms involved and the effective therapeutic targets for IDD. Recently, interleukin (IL)-1β has been recognized as an essential inflammatory factor and a key mediator of the inflammatory process in IDD. Current studies have found that IL-1β is mainly involved in IDD by affecting the metabolism of the extracellular matrix and regulating cell death (RCD), such as apoptosis, pyroptosis, and ferroptosis (a new form of RCD). Although analysis of clinical samples from different laboratories confirmed how IL-1β is induced in IDD, its specific signal transduction pathway, and the inflammatory role mediated in IDD remains unclear. This review describes the molecules and mechanisms involved in IL-1β-mediated inflammatory responses, and their roles in resolving the inflammatory process in IDD. Understanding the signaling pathways involved in IL-1β may lead to a new class of targets that promote remission for IDD patients. This review aims to provide a framework for the treatment of IDD by analyzing the signaling mechanism and function related to IL-1β, especially in terms of inflammation, matrix metabolism, and cell death regulation.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.